Norepinephrine/phenylephrine/vasopressin

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An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 42-year-old woman exhibited lack of efficacy during treatment with norepinephrine, vasopressin and phenylephrine. Additionally, she developed Takotsubo cardiomyopathy during the treatment with norepinephrine for the persistent hypotension [routes, dosages and duration of treatment to reactions onsets not stated].

The woman presented to a hospital from a nursing home with one week history of worsening mental status and fever. Her medical history was significant for Crohn's disease (under treatment with vedolizumab) and Guillain-Barr'e syndrome (GBS). At the time of admission to the emergency department, examinations showed BP of 93/62mm Hg, HR of 139 beats/min, temperature 38.2°C and oxygen saturation of 89% on 15 L/min. Lung examinations were notable for diffuse crackles without any cardiac murmurs. A chest x-ray showed normal cardiac silhouette with patchy consolidative opacities in the lung fields. ECG showed low voltage in the limb leads. A transthoracic echocardiography showed hyperdynamic left ventricle and a haemodynamically significant moderate-sized pericardial effusion with right atrial systolic collapse along with mild variability between the mitral valve and tricuspid valve inflow velocities. She received aggressive fluid resuscitation, but hypotension persisted. She then underwent emergent pericardiocentesis, but only 65mL of serous fluid was removed. Repeat transthoracic echocardiography persistent hypotension, which persisted despite the administration of high dose norepinephrine [Levophed] along with vasopressin and phenylephrine indicating lack of efficacy. Also, her ejection fraction reduced to 20%. Based on the examinations, a diagnosis of Takotsubo cardiomyopathy was made. Also, pericardial fluid sent for bacterial culture, acid fast bacilli smear and fungal culture yielded negative results. Serum inflammatory makers were noted as elevated and peak troponin level was mildly abnormal. For acute respiratory distress syndrome from fulminant pneumonia, unspecified broad spectrum antibacterials were started. She then underwent left heart catheterization for severely reduced ejection fraction, which showed normal coronaries with mildly increased left ventricular end diastolic pressure. For maximal support, an intra-aortic balloon pump was placed as a bridge. Due to persistent hypotension, norepinephrine (at a high dose), vasopressin and phenylephrine were continued; however, she continued to have refractory hypoxia despite ventilator optimization. Hence, she was transferred to a tertiary care center for consideration of advanced circulatory support. She was closely monitored in the ICU for the following 48 hours during which a diagnosis of COVID-19 infection was made. Her clinical condition continued to deteriorate, and she developed multiorgan failure and cardiogenic shock with anuric renal failure, and bowel ischaemia. Due to her poor prognosis, her family decided to place her on comfort measures. She passed away the same day. The Takotsubo cardiomyopathy was considered as secondary to the COVID-19 infection, but high dose norepinephrine therapy was also considered as a possible contributor.